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The present study was performed to determine whether the effects of ischemic preconditioning are mediated by a decrease in myocardial contractile activity or by a change in catabolite accumulation during the subsequent period of sustained ischemia. In ischemic preconditioning groups, crystalloid perfused rat hearts were subjected to 5 or 10 min of global ischemia before a 15-min reperfusion period and a subsequent 30 min period of ischemia, Non-preconditioned control hearts underwent a single 30-min ischemic period. In the 5-min preconditioned hearts, the onset of myocardial contracture was significantly delayed (22.0 +/- 1.6 min) compared with that in control hearts (14.7 +/- 0.7 min). Tissue ATP content of the myocardium during sustained ischemia was preserved better in 5-min preconditioned hearts than in control hearts. The time to contractile arrest during the sustained ischemic period was greater in the preconditioned hearts (3.9 +/- 0.3 and 3.1 +/- 0.2 min in PC5 and PC10 hearts respectively) than in controls (1.9 +/- 0.1 min). Thus, residual myocardial work during sustained ischemia (as estimated by the rate pressure product) was not decreased in the preconditioned hearts compared with that in control hearts. Extracellular acidosis was identical among the three groups during the subsequent period of sustained ischemia. The early rise in extracellular K+ during sustained ischemia progressively increased with the duration of preconditioning. We conclude that, in crystalloid perfused rat heart, 5 min of global ischemia had a salutary effect against cell damage caused by sustained ischemia. This "preconditioning" effect cannot be attributed to decreased myocardial work during ischemia nor to differences in extracellular H+ or K+ accumulation.

Effect of ischemic preconditioning on ischemia-induced contractile failure and accumulation of extracellular H+ and K+.